Acute Myocardial Infarction (AMI), a common disease that can have serious consequences, occurs when myocardial blood flow stops due to occlusion of the coronary artery. Early and accurate prediction of AMI is critical for rapid prognosis and improved patient outcomes. Metabolomics, the study of small molecules within biological systems, is an effective tool used to discover biomarkers associated with many diseases. This study intended to construct a predictive model for AMI utilizing metabolomics data and an explainable machine learning approach called Explainable Boosting Machines (EBM). The EBM model was trained on a dataset of 102 prognostic metabolites gathered from 99 individuals, including 34 healthy controls and 65 AMI patients. After a comprehensive data preprocessing, 21 metabolites were determined as the candidate predictors to predict AMI. The EBM model displayed satisfactory performance in predicting AMI, with various classification performance metrics. The model\'s predictions were based on the combined effects of individual metabolites and their interactions. In this context, the results obtained in two different EBM modeling, including both only individual metabolite features and their interaction effects, were discussed. The most important predictors included creatinine, nicotinamide, and isocitrate. These metabolites are involved in different biological activities, such as energy metabolism, DNA repair, and cellular signaling. The results demonstrate the potential of the combination of metabolomics and the EBM model in constructing reliable and interpretable prediction outputs for AMI. The discussed metabolite biomarkers may assist in early diagnosis, risk assessment, and personalized treatment methods for AMI patients. This study successfully developed a pipeline incorporating extensive data preprocessing and the EBM model to identify potential metabolite biomarkers for predicting AMI. The EBM model, with its ability to incorporate interaction terms, demonstrated satisfactory classification performance and revealed significant metabolite interactions that could be valuable in assessing AMI risk. However, the results obtained from this study should be validated with studies to be carried out in larger and well-defined samples.

There is currently little research on the effects of reduced left ventricular ejection fraction and altered nutritional status in patients with acute myocardial infarction. We therefore examined the interrelationship between the parameters of left ventricular dysfunction after acute myocardial infarction and changes in the Geriatric Nutrition Risk Index (GNRI) and the Nutrition Status Control Index (CONUT). Based on the evidence, frailty is considered to be an important factor affecting the prognosis of cardiovascular disease, so it is important to detect malnutrition early to prevent adverse cardiovascular events. This study was an observational, prospective study that included a total of 73 subjects who presented at the 3-month AMI follow-up. All subjects were subjected to laboratory tests and the groups were divided as follows: group 1, in which we calculated the CONUT score, (CONUT < 3 points, n = 57) patients with normal nutritional status and patients with moderate to severe nutritional deficiency (CONUT ≥ 3, n = 16). In group 2, the GNRI score was calculated and out of the 73 patients we had: GNRI ≥ 98, n = 50, patients with normal nutritional status, and GNRI < 98, n = 23, patients with altered nutritional status. The results of this study showed that we had significant differences between LVEF values at 3 months post-infarction where, in the CONUT group, patients with altered nutritional status had lower LVEF values (46.63 ± 3.27% versus 42.94 ± 2.54%, p < 0.001) compared to CONUT < 3. Also, in the GNRI group, we had lower LVEF values in patients with impaired nutritional status (46.48 ± 3.35% versus 44.39 ± 3.35%, p = 0.01). It can be seen that LVEF values are improved at 3 months post infarction in both groups, in patients with impaired nutritional status and in patients with good nutritional status. Patients with impaired nutritional status have lower ejection fraction and worse outcomes in both the CONUT and GNRI groups at 3 months post acute myocardial infarction.

Background: Early discharge following ST-segment-elevation myocardial infarction (STEMI) confers notable advantages for both patients and healthcare systems. However, the adoption of a very early discharge strategy for selected patients remains limited due to safety considerations. We aimed to provide some insight into the safety of a discharge program with a hospital stay lasting <48 h after a primary percutaneous coronary intervention (PCI). Methods: Using a registry of 1105 patients undergoing primary PCI for STEMI in our hospital between January 2015 and October 2023, we enrolled all the patients who had a hospital stay ≤48 h, according to a prespecified institutional protocol. The primary objective was a combined rate of non-fatal stroke, non-fatal acute myocardial infarction, or cardiovascular death within 30 days of discharge. Emergency department visits or hospitalizations due to cardiovascular causes, along with the all-cause mortality, were measured during the same period. Results: A total of 453 (41%) patients were discharged ≤48 h after admission for a STEMI. The mean age was 62.4 (±12.5 years), 24.3% were women, and 17.9% were people with diabetes. Up to 96% of the procedures had been performed through radial artery access, and there were no major vascular complications. Regarding the primary endpoint, there was one event (0.2%; one patient suffered a non-fatal myocardial infarction). There were no cardiovascular deaths or deaths from other causes. Only five patients (1.1%) were re-hospitalized or visited the emergency department due to cardiovascular causes. Conclusions: An early discharge strategy for patients within 48 h of experiencing STEMI and undergoing primary PCI appears feasible and safe.

Background: Specifically young women are at risk for a poor outcome after ST-elevation myocardial infarction (STEMI). We aimed to investigate sex- and age-specific differences in outcome and associate these results with adherence to a guideline-directed optimal medical therapy (OMT). Methods: Administrative insurance data (≈26 million insured) were screened for patients aged 18-60 years with STEMI. Patient demographics, details on in-hospital treatment, adherence to OMT and its effect on mortality were assessed. Adherence to OMT was analyzed using multistate models and an association of those with death was fitted using multivariable Cox regression models with time-dependent co-variables. Results: Overall, 59,401 patients (19.3% women), median age 52 (interquartile range 48, 56) presented with STEMI. Female sex was associated with a poor outcome early after STEMI (90-day mortality: odds ratio 1.22, 95% confidence interval (CI) 1.12-1.32, p < 0.001). Overall survival was reduced in women compared to same-aged men. The ten-year survival rate was 19.7% (18.1-21.2%) versus 19.6% (18.9-20.4%) in men (p < 0.001). Although long-term drug adherence was low, its intake was associated with a better outcome. Specifically younger women showed a markedly lower mortality when on OMT (hazard ratio (HR) 0.22 (95% CI 0.19-0.26) versus HR 0.31 (95% CI 0.28-0.33) in men, pint < 0.001). Conclusions: Specifically young women were at risk for a poor outcome in the early phase after STEMI. Although long-term adherence to OMT was low, it was generally associated with a lower mortality, specifically in women. Our findings emphasize on early and long-term preventive measures in all patients after STEMI.

BACKGROUND: Previous studies evaluating the association between prediabetes the prognosis of patients with acute myocardial infarction (AMI) showed inconsistent results. The aim of the meta-analysis was to compare the long-term incidence of major adverse cardiovascular events (MACEs) between AMI patients with prediabetes and normoglycemia.
METHODS: Relevant prospective cohort studies were obtained by searching Medline, Web of Science, and Embase databases. Only studies with follow-up duration of at least one year were included. A random-effects model was utilized to pool the results by incorporating the influence of heterogeneity.
RESULTS: Twelve studies with 6972 patients with AMI were included. Among them, 2998 were with prediabetes and 3974 were with normoglycemia. During a mean follow-up of 52.6 months, 2100 patients developed MACEs. Compared to those with normoglycemia, AMI patients with prediabetes were associated with a higher incidence of MACEs (risk ratio [RR]: 1.30, 95% confidence interval: 1.07 to 1.58, p = 0.008; I2 = 67%). Subgroup analysis showed a stronger association between prediabetes and MACEs in studies of patients with mean age ≥ 60 years compared to < 60 years (RR: 1.66 versus 1.10, p for subgroup difference = 0.04), with proportion of men < 75% compared to ≥ 75% (RR: 1.87 versus 1.08, p for subgroup difference = 0.01), and in prediabetes evaluated at or after discharge compared to that evaluated within three days of AMI onset (RR: 1.39 versus 0.78, p for subgroup difference = 0.01).
CONCLUSIONS: Prediabetes may be associated with a higher risk of MACEs in patients with AMI.

Subsequently to the publication of the above article, the authors have realized that, in Fig. 1A, the incorrect image was uploaded to show the ultrastructure of exos isolated from plasma and examined using transmission electron microscopy (essentially, the image in question had already appeared in an article published by the same research group in Journal of Cellular and Molecular Medicine). In addition,  the \'+\' and \'-\' signs for the \'Cell lysis\' experiments shown underneath the gels in Fig. 1B were incorporated the wrong way around. The revised version of Fig. 1, showing the correct image in Fig. 1A and the correct labels in Fig. 1B, is shown below. Note that the errors made in assembling this figure did not have a major impact on either the results or the conclusions reported in this paper. The authors are grateful to the Editor of Molecular Medicine Reports for allowing them this opportunity to publish a corrigendum, and apologize to the readership of the Journal for any inconvenience caused. [Molecular Medicine Reports 27: 124, 2023; DOI: 10.3892/mmr.2023.13010].

UNASSIGNED: Contrast-induced nephropathy (CIN) is a common post-procedural complication of percutaneous coronary intervention for acute myocardial infarction (AMI). Anisodamine hydrobromide is an alkaloid that has demonstrated efficacy in improving microcirculation. This meta-analysis aims to evaluate the reno-protective effects of Anisodamine in patients undergoing percutaneous coronary intervention (PCI) for AMI.
UNASSIGNED: PubMed, Embase, Cochrane Library, Scopus, and clinicaltrials.gov were searched from inception to January 2024 for randomized controlled trials (RCTs) comparing the efficacy of Anisodamine in preventing the development of CIN. Outcomes of interest included the incidence of CIN, serum creatinine levels, and estimated glomerular filtration rate (eGFR). A random-effects model was used for pooling standard mean differences (SMDs) and odds ratios (ORs) with a 95% CI. Statistical significance was considered at a P less than 0.05.
UNASSIGNED: Three RCTs involving 563 patients were included. Anisodamine was associated with a reduction in the incidence of CIN [OR: 0.44; 95% CI: 0.28, 0.69; P=0.0003], a reduction in serum creatinine levels at 48 [SMD: -6.78; 95% CI: -10.54,-3.02; P=0.0004] and 72 h [SMD: -6.74; 95% CI: -13.33,-0.15; P=0.03], and a higher eGFR at 24 [SMD: 5.77; 95% CI: 0.39, 11.14; P=0.03], and 48 h [SMD: 4.70; 95% CI: 2.03,7.38; P=0.0006]. The levels of serum creatinine at 24 h and eGFR value at 72 h were comparable between both groups.
UNASSIGNED: Anisodamine has demonstrated clinical efficacy in ameliorating the development of CIN post-PCI in AMI patients. Large, multi-centric RCTs are warranted to evaluate the robustness of these findings.

Background: This study investigated the prognostic value of cardiovascular magnetic resonance (CMR)-derived global coronary flow reserve (G-CFR) in addition to cardiopulmonary exercise testing (CPET) variables in patients with acute myocardial infarction (AMI). Methods and Results: We investigated 127 patients with AMI who underwent primary or urgent percutaneous coronary intervention (PCI) and post-intervention CMR and CPET. The incidence of major cardiac and cerebrovascular events (MACCE), defined as all-cause death, recurrent non-fatal myocardial infarction, re-hospitalization due to congestive heart failure, and stroke, was evaluated (median follow-up, 2.8 years). Patients with MACCE (n=14) had lower ejection fraction (EF) (50 [43-59] vs. 58 [51-63]%; P=0.014), lower G-CFR (1.74 [1.19-2.20] vs. 2.40 [1.61-3.66]; P=0.008), and lower peak oxygen consumption (V̇O2) (15.16±2.64 vs. 17.19±3.70 mL/kg/min; P=0.049) than patients without MACCE. G-CFR<2.33 and peak V̇O2 <15.65 mL/kg/min (cut-off values derived from receiver operating characteristic curve analyses) were significantly associated with the incidence of MACCE (log-rank test, P=0.01). The combination of low G-CFR and low peak V̇O2 improved risk discrimination for MACCE when added to the reference clinical model including age, male sex, post-PCI peak creatine kinase, EF, and left anterior descending artery culprit lesion. Conclusions: G-CFR and peak V̇O2 showed incremental prognostic information compared with the reference model using historically important clinical risk factors, indicating that this approach may help identify high-risk patients who suffer subsequent adverse events.

Background: Older adults with acute myocardial infarction (AMI) are currently a rapidly growing population. However, their clinical presentation and outcomes remain unresolved. Methods and Results: A total of 268 consecutive AMI patients were analyzed for clinical characteristics and outcomes with major adverse cardiovascular events (MACE) and all-cause mortality within 1 year. Patients aged ≥80 years (Over-80; n=100) were compared with those aged ≤79 years (Under-79; n=168). (1) Primary percutaneous coronary intervention (PCI) was frequently and similarly performed in both the Over-80 group and the Under-79 group (86% vs. 89%; P=0.52). (2) Killip class III-IV (P<0.01), in-hospital mortality (P<0.01), MACE (P=0.03) and all-cause mortality (P<0.01) were more prevalent in the Over-80 group than in the Under-79 group. (3) In the Over-80 group, frail patients showed a significantly worse clinical outcome compared with non-frail patients. (4) Multivariate analysis revealed Killip class III-IV was associated with MACE (odds ratio [OR]=3.51; P=0.02) and all-cause mortality (OR=9.49; P<0.01) in the Over-80 group. PCI was inversely associated with all-cause mortality (OR=0.13; P=0.02) in the Over-80 group. Conclusions: The rate of primary PCI did not decline with age. Although octogenarians/nonagenarians showed more severe clinical presentation and worse short-term outcomes compared with younger patients, particularly in those with frailty, the prognosis may be improved by early invasive strategy even in these very old patients.

Long non-coding RNA RP11-64B16.4 (myocardial infarction protection-related lncRNA [MIPRL]) is among the most abundant and the most upregulated lncRNAs in ischemic human hearts. However, its role in ischemic heart disease is unknown. We found MIPRL was conserved between human and mouse and its expression was increased in mouse hearts after acute myocardial infarction (AMI) and in cultured human and mouse cardiomyocytes after hypoxia. The infarcted size, cardiac cell apoptosis, cardiac dysfunction, and cardiac fibrosis were aggravated in MIPRL knockout mice after AMI. The above adverse results could be reversed by re-expression of MIPRL via adenovirus expressing MIPRL. Both in vitro and in vivo, we identified that heat shock protein beta-8 (HSPB8) was a target gene of MIPRL, which was involved in MIPRL-mediated anti-apoptotic effects on cardiomyocytes. We further discovered that MIPRL could combine with the messenger RNA (mRNA) of HSPB8 and increase its expression in cardiomyocytes by enhancing the stability of HSPB8 mRNA. In summary, we have found for the first time that the ischemia-enhanced lncRNA MIPRL protects against AMI via its target gene HSPB8. MIPRL might be a novel promising therapeutic target for ischemic heart diseases such as AMI.